ReviewInternational journal of molecular sciences2023
p53 and Myofibroblast Apoptosis in Organ Fibrosis.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- ECM-Stiffness Mediated Persistent Fibroblast Activation Requires Integrin and Formin Dependent Chromatin Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- MFN2 Overexpression Attenuates Coal Dust-Induced Pulmonary Fibrosis by Modulating MAMs Integrity and Cell Apoptosis.Toxics · 2026Article
- The Fibro-Immune Landscape Across Organs: A Single-Cell Comparative Study of Human Fibrotic Diseases.International journal of molecular sciences · 2026Article
- Therapeutic Potential of Cannabinoids in Attenuating Amiodarone-Induced Pulmonary Fibrosis: An in vivo Experimental Study in Wistar Rats.Drug design, development and therapy · 2026Article
- Molecular insights of a Unani formulation in targeting fibrosis-associated diseases.Frontiers in pharmacology · 2026Review
- Transcriptomic Insights into Tumor Necrosis Factor α's Role in the Fibrosis-Related Processes of Equine Endometrial Fibroblasts.International journal of molecular sciences · 2025Article
- [Effect and mechanism of astaxanthin on the aging of high glucose-treated human skin fibroblasts].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2025Article
- The interplay of senescence and MMPs in myocardial infarction: implications for cardiac aging and therapeutics.Biogerontology · 2025Review
- Leveraging Microneedles for Raised Scar Management.Polymers · 2025Review
- Identification and validation of biomarkers, construction of diagnostic models, and investigation of immunological infiltration characteristics for idiopathic frozen shoulder.Frontiers in immunology · 2025Article
- Network pharmacology and experiments verify the effect of triptolide on extraocular muscle fibrosis.PloS one · 2025Article
- p53 and the E3 Ubiquitin Ligase MDM2 in Glaucomatous Lamina Cribrosa Cells.International journal of molecular sciences · 2024Article
- Renal Fibrosis: SIRT1 Still of Value.Biomedicines · 2024Review
- Article
- The Role of Vimentin in Human Corneal Fibroblast Spreading and Myofibroblast Transformation.Cells · 2024Article
- ROS-induced imbalance of the miR-34a-5p/SIRT1/p53 axis triggers chronic chondrocyte injury and inflammation.Heliyon · 2024Article
- Advances in Nanoparticles in the Prevention and Treatment of Myocardial Infarction.Molecules (Basel, Switzerland) · 2024Review
- Genome-wide RNA sequencing of ocular fibroblasts from glaucomatous and normal eyes: Implications for glaucoma management.PloS one · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Organ fibrosis represents a dysregulated, maladaptive wound repair response that results in progressive disruption of normal tissue architecture leading to detrimental deterioration in physiological function, and significant morbidity/mortality. Fibrosis is thought to contribute to nearly 50% of all deaths in the Western world with current treatment modalities effective in slowing disease progression but not effective in restoring organ function or reversing fibrotic changes. When physiological wound repair is complete, myofibroblasts are programmed to undergo cell death and self-clearance, however, in fibrosis there is a characteristic absence of myofibroblast apoptosis. It has been shown that in fibrosis, myofibroblasts adopt an apoptotic-resistant, highly proliferative phenotype leading to persistent myofibroblast activation and perpetuation of the fibrotic disease process. Recently, this pathological adaptation has been linked to dysregulated expression of tumour suppressor gene p53. In this review, we discuss p53 dysregulation and apoptotic failure in myofibroblasts and demonstrate its consistent link to fibrotic disease development in all types of organ fibrosis. An enhanced understanding of the role of p53 dysregulation and myofibroblast apoptosis may aid in future novel therapeutic and/or diagnostic strategies in organ fibrosis.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.